Congestive Heart failure is defined as the failure of the heart to pump blood at a rate to satisfy the requirements of metabolizing tissues. Heart failure is the manifestation of many disease processes affecting the heart and the great vessels, including ischemic cardiomyopathy, viral cardiomyopathy, metabolic or toxic cardiomyopathy and idiopathic cardiomyopathy. Many of these disease processes lead to dilation of the left ventricle as an initial adaptive or compensatory mechanism. This is a short-lived adaptation due to the impaired contractile function of the heart with an inappropriate thinning of myocardium rather than appropriate thickening and, thereby, leading to further left ventricle dilation and cardiac deterioration.
Congestive heart failure is a leading cause of death in the United States. With the aging of the population (baby boomers) and the advent of improved cardiovascular therapies, the incidence of congestive heart failure is increasing. Congestive heart failure is most prevalent in people of age 65 or older (incidence 3/1,000 in men age 50-59 and 27/1000 in men age 80-89) and, by 2030, it is estimated that heart failure prevalence will double to 5.7 million cases annually, thereby reaching pandemic proportions. See Starling (1998) The Heart Failure Pandemic: Changing Patterns, Cost, and Treatment Strategies. Cleveland Clinic Journal of Medicine, 65:351-358. Within the next ten years it is estimated that 70 million Americans will suffer from congestive heart failure.
As the disease of congestive heart failure progresses the left ventricle further dilates, and the myocardial wall thickness is further diminished. In addition, the left ventricle becomes more spherical and less episoidal, the distance between the papillary muscles and the mitral annulus increases, and the mitral annulus enlarges, especially in the anterior/posterior direction resulting in significant mitral regurgitation. The thinning of the left ventricular myocardium significantly and progressively raises the stress level in the left ventricular wall such that left ventricle function is diminished and eventually ceases to provide sufficient cardiac output to sustain life, resulting in the demise of the patient.
Typically in congestive heart disease the internal diameter of the ventricle increases over time and the left ventricular wall thickness decrease over time. In some patients the systolic pressure increases due to systemic hypertension or aortic stenosis. A similar scenario occurs, but for different reasons, in patients with mitral valve regurgitation and concomitant aortic stenosis or systemic hypertension.
In the last two decades there have been significant advances in medical management of congestive heart failure. However, despite these significant improvements in clinical outcomes (death and quality of life) of congestive heart failure, these therapies are limited and as the disease relentlessly progresses the patient either needs to receive a cardiac transplant or will die. Cardiac transplantation presently is the treatment of choice for medically refractory congestive heart failure. Donor organ shortages and patient selection (eligibility) limit this therapy to only a relatively low percentage of patients.
Several problems face the clinician in treating patients with congestive heart failure. The first concern is the determination of how far the disease has progressed. The second concerns when the patient has become a viable candidate for surgery, either for cardiac transplantation or alternative surgical intervention.
Preload (length of stretch of sarcomere at end of diastole) and after load (wall stress during ventricular ejection) are interdependent and physiologic components of heart function. See Braunwald ed., (1992) Heart Disease: A Textbook of Cardiovascular Medicine, 4th edition. W.B. Saunders and Company, Philadelphia, p. 370-382. Many pharmacological therapies have targeted their efficacy on these parameters by reducing ventricular volumes or cardiac and systemic pressures while other therapies alter the inotropic (contractile force) function of the heart. Medical therapy (neuroendocrine axis, improved expression of contractile proteins, enhanced cellular respiratory control, and decrease in markers of apoptosis and cellular stress) however, has had limited success, not only with the management of symptoms but also in achieving long-term survival benefit.
In an attempt to counter the progression of congestive heart failure, in 1996 Batista, recognizing the relentless progression of the disease, described a surgical procedure in which a segment of the left ventricle was removed, thus reducing the overall internal diameter of the heart. See J. Card. Surg. 1996 March-April; 11(2):96-7. Of course, the operative procedure also removed a segment of potentially contractile myocardium, reducing the overall contractive potential of the heart as a whole.
Presently, surgical intervention generally consists of a surgical remodeling of the left ventricle to reduce its end-diastolic volume and attempting to re-convert the abnormal spherical shaped ventricle to the near normal elipisoidal shaped ventricle. However, this usually means the implantation of an akinetic ventricular patch, so the patient's ventricular ejection fraction is seldom normal following surgery. In patients where the mitral annulus has become greatly distorted, usually by elongation, it is necessary to implant a rigid type mitral annuloplasty ring. This surgery, although helpful in some patients, is not fully effective.
End diastolic external cardiac restricting devices have been used in an attempt to prevent spherical distortion or enlargement of ventricles. For example, Acorn Cardiovascular, Inc. sells CorCap™, an endocardial support device, which is a mesh-like heart “jacket” that is placed around the heart and held in place to prevent any further enlargement (See U.S. Pat. Nos. 6,582,355; 6,579,226; 6,537,203). This and similar devices, although providing immediately post-operative effective relief for the patient, may lead to long term constrictive pericarditis in a significant number of patients. Another end diastolic restricting device has been proposed by Vidlund R M et al. (See U.S. Pat. No. 6,537,198). This patent discloses using one or more cables passed through opposing portions of the myocardial wall and across the ventricular cavity to exit the opposing myocardial wall. Ends of the cable are intended to be secured using crimped “buttons”. This proposed method may not provide sufficient myocardial support to the heart.
Alternative mechanical devices are, therefore, necessary and needed. See Gregoric and Couto (2002) Surgical Treatment of Congestive Heart Failure, Congestive Heart Failure, 8:214-219 Many end-stage congestive heart failure patients may, therefore, benefit from a mechanical device, either as a bridge to transplant or as destination therapy, if they are otherwise ineligible for transplant. See Nemeh and Smedira (2003) Mechanical Treatment of Heart Failure: The Growing Role of LVADs and Artificial Hearts, Cleveland Clinic Journal of Medicine 70:223-233; see also Westaby (1996) The Need for Artificial Hearts, Heart, 76:200-206.
Each of the foregoing patents and publications is incorporated herein by reference in its entirety. The present invention is intended to address one or more of the problems discussed herein.